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kidnapping, or torture. The criteria were later altered to include more common
traumatic events, such as car accidents and crime victimization (Summerfi eld,
2001), as experienced by A. C. in Case 7.7.- The criteria were altered for DSM-IV so that “second-hand victimization” is
possible—that is, hearing about a traumatic event qualifi es as having experi-
enced it (McNally, 2003; Spitzer, First, & Wakefi eld, 2007). - What originally started as a way to understand war-related stress symptoms
among soldiers has become something else—a way to seek the status of “victim”
(Summerfi eld, 2001) for legal, fi nancial, or psychological reasons (Spitzer, First,
& Wakefi eld, 2007). - PTSD is the only diagnosis for which people can sue for compensation (Mezey &
Robbins, 2001). Critics have claimed that the existence of a fi nancial incentive
means that PTSD is overdiagnosed, and people are intentionally or inadver-
tently encouraged to report being more traumatized than they really are (Mezey &
Robbins, 2001; Spitzer, First, & Wakefi eld, 2007). Support for this claim comes
from surveys that have found substantially lower rates of PTSD in people out-
side North America (Creamer, Burgess, & McFarlane, 2001; Perkonigg
et al., 2000).
Taken together, these criticisms indicate that not all researchers agree with theDSM-IV-TR defi nition of a traumatic event or the specifi c diagnostic criteria for PTSD.
Understanding Posttraumatic Stress Disorder
Given that most people who experience a trauma do not go on to develop PTSD,
the neuropsychosocial approach can help explain how neurological, psychological,
and social factors can infl uence each other in particular ways and lead to PTSD.
The various factors that contribute to PTSD may arise before the trauma, during
the trauma, or after the trauma. Some form of combat-related stress disorder has
been recognized for many decades, even centuries, giving researchers clues about
possible factors to investigate more systematically.
Targeting Neurological Factors
The neurological factors that contribute to PTSD appear to arise, in large part, from
interactions between the frontal lobe and the amygdala. In addition, the neurotrans-
mitters norepinephrine and serotonin have been implicated in the disorder, and there
is evidence that genes contribute to (but by no means determine) the likelihood that
experiencing trauma will result in PTSD.
Brain Systems
Research has often shown that PTSD sufferers react more strongly to cues that they
associate with their traumatic experience than do others. The cues can cause sweat-
ing or a racing heart (Orr, Metzger, & Pitman, 2002; Orr et al., 1993; Prins, Kaloupek, &
Keane, 1995). Furthermore, the changes in heart rate are distinct from the changes
found in control participants who have been asked to pretend having PTSD (Orr &
Pitman, 1993). Thus, PTSD patients are not simply pretending, but do in fact react
more strongly to the relevant cues than would be expected if they did not have a
disorder.
In an effort to chart the mechanisms that give rise to these reactions, research-ers have studied the brains of PTSD patients. First, MRI studies have shown that
PTSD patients have smaller hippocampi than control participants (Bremner et al.,
1995, 1997, 2003). Combat veterans with PTSD also had smaller hippocampi than
other combat veterans who did not have PTSD (Gurvits et al., 1996). Second, the
hippocampus apparently must work harder than normal in PTSD patients when
they try to remember information, as shown by the fact that it is more strongly acti-
vated in these patients during memory tasks than in control participants (Shin et al.,